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首页> 外文期刊>American Journal of Physiology >Contribution to sympathetic vasomotor tone of tonic glutamatergic inputs to neurons in the RVLM.
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Contribution to sympathetic vasomotor tone of tonic glutamatergic inputs to neurons in the RVLM.

机译：对RVLM中神经元的强直性谷氨酸能输入的交感性血管舒缩张力的贡献。

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摘要

The role of excitatory amino acid (EAA) receptors in the rostral ventrolateral medulla (RVLM) in maintaining resting sympathetic vasomotor tone remains unclear. It has been proposed that EAA receptors in the RVLM mediate excitatory inputs both to presympathetic neurons and to interneurons in the caudal ventrolateral medulla (CVLM), which then provide a counterbalancing inhibition of RVLM presympathetic neurons. In this study, we tested this hypothesis by determining the effect of blockade of EAA receptors in the RVLM on mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), after inhibition of CVLM neurons. In anesthetized rats, bilateral injections of muscimol in the CVLM increased MAP, HR, and RSNA. Subsequent bilateral injections of kynurenic acid (Kyn, 2.7 nmol) in the RVLM caused a modest reduction of approximately 20 mmHg in the MAP but had no effect, when compared with the effect of vehicle injection alone, on HR or RSNA. By approximately 50 min after the injections of Kyn or vehicle in the RVLM, the MAP had stabilized at a level close to its original baseline level, but the HR and RSNA stabilized at levels above baseline. The results indicate that removal of tonic EAA drive to RVLM neurons has little effect on the tonic activity of RVLM presympathetic neurons, even when inputs from the CVLM are blocked. Thus the tonic activity of RVLM presympathetic neurons under these conditions is dependent on excitatory synaptic inputs mediated by non-EAA receptors and/or the autoactivity of these neurons.
机译：目前尚不清楚兴奋性氨基酸（EAA）受体在延髓腹侧延髓（RVLM）中维持静止的交感性血管舒缩张力的作用。已经提出，RVLM中的EAA受体介导交感神经输入到交感神经前神经元和尾侧腹外侧延髓（CVLM）的中间神经元，然后提供对RVLM交感神经元的平衡抑制。在这项研究中，我们通过确定抑制CVLM神经元后，确定RVLM中EAA受体的阻断对平均动脉压（MAP），心率（HR）和肾交感神经活性（RSNA）的影响，验证了这一假设。在麻醉的大鼠中，在CVLM中双侧注射麝香酚可增加MAP，HR和RSNA。随后在RVLM中双侧注射犬尿酸（Kyn，2.7 nmol），可使MAP适度降低约20 mmHg，但与单独注射赋形剂相比，对HR或RSNA没有影响。在RVLM中注射Kyn或媒介物后约50分钟，MAP稳定在接近其原始基线水平的水平，但HR和RSNA稳定在基线之上的水平。结果表明，即使对CVLM的输入被阻止，去除对RVLM神经元的滋补EAA驱动也不会对RVLM前交感神经元的滋补活性产生影响。因此，在这些条件下RVLM交感神经元的强直活动取决于非EAA受体介导的兴奋性突触输入和/或这些神经元的自发活动。

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